Collectively, VEGF-, PARP-, and FRα-targeted therapies have enabled more rational treatment sequencing, informed combination strategies, and personalized clinical decision-making in ovarian cancer. Ongoing efforts to define optimal sequencing, overcome acquired resistance, and refine predictive biomarkers are expected to further enhance the durability and breadth of benefit from targeted therapies and advance precision oncology in gynecologic malignancies.
GTN exhibits frequent expression of several established ADC targets, particularly Nectin4 and FOLR1. These findings provide a molecular rationale for biomarker-driven investigation of ADC-based therapeutic strategies in refractory or recurrent GTN.
This combinatorial approach offers a promising strategy to overcome TME-mediated immunosuppression. These findings support further development of dual-targeting approaches to improve therapeutic outcomes in TNBC.
In a small heterogeneous group of heavily pretreated patients, general recommendations for therapy with MIRV are limited. Close collaboration with ophthalmology and patient education is essential to mitigate ocular events.
The broader-than-expected mutational landscape, including recurrent TP53 mutations, alterations in MAPK and PI3K pathways, and notable MYC amplification, further refines current understanding of TAS biology. These findings offer a basis for the development of prospective therapeutic strategies in this rare and aggressive malignancy.
Human FOLR1-VH CAR T cells demonstrated potent antitumor activity with reduced exhaustion and enhanced persistence. These properties highlight the VH domain as a promising targeting module for next-generation CAR T-cell therapies in ovarian cancer.
High FOLR1 expression identifies a biologically aggressive subset of gastric adenocarcinoma with inferior RFS and independent prognostic value. Its concurrent association with PD-L1 and HER2, together with relative absence in dMMR tumors, supports biomarker-guided strategies that consider FOLR1 alongside HER2 and PD-L1, and provides a rationale to explore FOLR1-targeted therapies in selected patients.
While TGF-β typically impairs NK cell function, our armed CAR-NK cells successfully infiltrated tumoroids and synergized with Trastuzumab to induce potent ADCC-mediated lysis. Our findings define the TGF-β/SMAD2 axis as a central driver of NK cell dysfunction in ovarian cancer and demonstrate that bi-specific CAR-NK platforms offer a robust therapeutic solution to bypass TME-induced suppression and restore antibody-mediated tumor suppression.